*Goat Immunity to Helminthes DOI: http://dx.doi.org/10.5772/intechopen.91189*

*Goats (Capra) - From Ancient to Modern*

from blood vessels [73].

**8. Host-parasite interaction**

(also labeled M2 cells) which occurred by the presence of helminth infection. This is driven by type 2 cytokines IL 4 and IL 13 cytokines (**Figure 3**). Ongoing research divided these Mϕ by gene expression, metabolism, and function differences into classically activated (M1) macrophages. However, M2 macrophages are required in the effective immunity to some parasites (including *H polygyrus*) [15]. The DCs are professional antigen-presenting cells (APCs) that play an essential role in presenting antigen to T cells to initiate immune responses. Although the role of DCs in inducing TH 1, TH 17, and Treg responses is well established. Often overshadowed by their T-cell counterparts, regulatory B (Breg) cells are also crucially important in

control of the immune response during helminth infection [15] (**Figure 8**).

These DCs can also patrol among enterocytes while extending dendrites towards the lumen [16]. Treg cell population by producing IL-10 to harness immune tolerance [98]. CX3CR1+ phagocytic cells can capture Salmonella by extending dendrites across epithelium in a CX3CR1-dependent manner [99]. Antigens captured by CX3CR1+ phagocytic cells can be transferred through gap junctions to CD103+ DCs in the lamina propria to establish oral tolerance [100]. In addition to luminal antigen, lamina propria CX3CR1+ cells facilitate the surveillance of circulatory antigens

Almost all animals get gastrointestinal infection (GI) by helminthes in their lifetime. Though all parasite (Helminthes) species share a very similar general morphology and they undergo into four molts reforms during their development period [101]. Each of the species shares dioeciously life spans that could be weeks to years. These worms are investigated because they threaten animal as well to the human health [102]. Nearly all helminthes invade tissues and install an immunomodulatory surrounding for their survival especially taking care of Treg cells [103]. Recently cites articles suggest that both, worms and host, evolved to get reciprocal immune related benefits during the disorders with some clinical outcomes. Numerous studies suggest that immune response appears to be imprisoned that is even extended to expansion of Treg cells [103]. As a consequent a melioration of type 2 immune response that resulted in chronicity [103]. Many findings, however, chronic helminth infection are still poorly understood. These parasites are also important as a model where they create constant, foremost challenge to host immune system [101]. Many of aspects, especially regulation of chronic GI infection, remain to be defined. It is believed that during the evolutionary processes they exclusive adapted to such avoidance to host defenses [104]. These masterful adaptations enable them to remodulate host immune response [105]. It may well be the evolutionary mechanisms that exclusively down regulates early expansion of ILC 2. This is seen in *Heligmosomoides polygyrus* system where IL 1β shows to down regulate early ILC 2 responses in mice [106]. However, this is not true for another parasitic *Trichuris muris* infection where IL 1β null mice [107]. This depression in the levels of IL 1β provokes type 2 protective immune responses, and leads to worm expulsion [53]. The helminthes in the GI tract interact with the mucus layer and many a times pass through into the epithelial layer and reproduce at the site [108]. One of the interaction of worms to intestinal mucosal barrier and hyperplasia, secretion large mucin forming a layer. The mucus layer is a highly hydrated gel mucins. These are largely high molecular weight glycosylated glycoproteins secreted by goblet cells (GCs). The initial also interact with antimicrobial compounds, commensal metabolites and finally antibodies. Like in mouse as well as in humans, MUC 2 cells produces to mucus layer as predominantly part first line of innate immune response [109].

**170**

Mucin production is synchronized by many immune type 2 cytokines. As discussed above, IL 4 and IL 13, plays key role in proliferation and differentiation of these GCs [101]. As the intestinal infection ensues it initiates worm expulsion seen for many helminthes [110]. This expulsion is influenced by the presence of CD 4 TH 2 cells which are controlled by IL 13 secretion [27]. In the knock down mutant studies in mouse showed that MUC 2, regulated by IL 13, led to defective delay in worm expulsion [101]. The, above described, incitation of type 2 immunity releases IL 4, IL 5, IL 9 and IL 13. Several other immune and nonimmune cell activators also participates in the web of effector mechanisms that also sways to parasite expulsion [111]. The commencement of the immune response by TH 2 cell trails through ILC 2 and subsets of dendritic cells. The sensed and trigger signals, however, of PAMP and DAMP results in the activation of different subsets of ILC 2 bundle, dendritic cells, various types of T cell types, basophils and nonimmune intestinal epithelial cells (IEC) against intestinal helminthes. The heterogeneous intestinal epithelium contains seven different cells that can sense helminth invasion into the epithelial cells to initiate TH 2 cell mediated immunity [103].
